Nonspecific Defenses of the Host
Chapter 16
I. Introduction: Overview of host defenses
• A. Resistance – Ability to ward off disease
through body defenses
– 1. Nonspecific – All body defenses that protect
one from any kind of pathogen. Includes the first
and second lines of defense.
– 2. Specific – Defenses against specific
microorganisms mediated by lymphocytes (white
blood cells) and special proteins called antibodies.
• B. Susceptibility – Lack of resistance that
creates host vulnerability.
Figure 16.1 - Overview (1 of 3)
II. Skin and Mucous Membranes
• A. Mechanical Factors – Include intact skin, keratin, lacrimal
apparatus of eye, saliva, mucous with ciliary escalator, and
urine.
II. Skin and Mucous Membranes
• A. Mechanical Factors – Include intact skin, keratin, lacrimal
apparatus of eye, saliva, mucous with ciliary escalator, and
urine.
II. Skin and Mucous Membranes
• B. Chemical Factors – Include sebaceous (oil) glands
secretion (sebum), perspiration, lysozyme (against GPC), high
acidity (pH skin = 3-5, gastric juice = 1-2).
• C. Normal flora compete with pathogens, establish
conditions unsuitable for pathogens, produce substances
harmful to pathogens.
Staph on skin
III. Phagocytosis
• Phagocytosis – Ingestion of a microorganism or particulate
matter by phagocytic cells.
• A. Formed Elements of the Blood – differential count of WBCs.
III. Phagocytosis
• B. Specific Kinds of Leukocytes:
– Granulocytes (3 types in the blood)
•
•
•
•
Neutrophils
Basophils
Eosinophils
Dendritic cells (found in lymph nodes, skin, etc. but not
in the blood)
– Agranulocytes (two types in the blood)
• Monocytes
• Lymphocytes- three population that appear similar
• Natural Killer (NK) cells
• B cells
• T cells
III. Phagocytosis
• B.
Specific Kinds of Leukocytes:
– Granny can’t
•
•
•
•
•
Basophils
Eosinophils
Neutrophils
Dendritic cells
She got
– Agranulocytes
•
•
•
•
Monocytes
Natural Killer (NK)ey
Bi
Te
III. Phagocytosis
• C. Action of Phagocytic Cells
– 1. Granulocytes migrate from blood to area of
infection and are phagocytic or dump granular
contents on pathogens. Eosinophils are often
prominent in parasitic infections.
– 2. Monocytes enter tissue and become fixed
macrophages and then have specific names
depending on area.
• Examples: dendritic cells-lymph nodes; Kupffer cellsliver; Langerhans-skin
– 3. Granulocytes (especially neutrophils) increase
the most first and then monocytes increase.
III. Phagocytosis
• C. Action of Phagocytic Cells
Macrophage engulfing rod shaped bacteria
III. Phagocytosis
• D. Mechanism of Phagocytosis
– Chemotaxis, adherence, ingestion, and digestion
III. Phagocytosis
• E. Inflammation – Bodily
response to cell damage
characterized by redness,
pain, heat, and swelling.
– 1. Three stages:
• tissue damage,
• vasodilation,
• phagocytosis.
– 2. Goal:
• destroy pathogen or limit
infection,
• then repair damage.
Fig 16.8 Process of inflammation
III. Phagocytosis
• F. Fever – One of the systemic responses to infection
– 1. Caused (primarily) by endotoxins released by
gram-negative cell walls or viruses.
– 2. Endotoxins cause phagocytes to produce IL-1,
which acts on the hypothalamus (body’s
thermostat).
– 3. Hypothalamus releases prostaglandins that reset
the temperature of the body to a higher
temperature, thus causing fever via vessel
constriction and shivering. As fever breaks,
vasodilation and sweating occurs, so skin becomes
warm.
III. Phagocytosis
• G. Antimicrobial Substances
– 1.
Complement System:
• A set of cascading serum proteins (30 or so) that
participate in lysis of foreign cells, inflammation, and
phagocytosis.
• Outcomes: inflammation, cytolysis, opsonization
(immune adherence)
• See overview next slide fig 16.9, 16.10
Outcomes of complement activation
Figure 16.9 - Overview (1 of 5)
Cytolysis caused by complement
Figure 16.10 - Overview (1 of 3)
III. Phagocytosis
• G. Antimicrobial Substances
– 1. Complement System
• a. Classic Pathway
• Can assist specific
immunity (complement).
initiated by antigenantibody reaction
III. Phagocytosis
• G.
Antimicrobial Substances
– 1.Complement System
• b. Nonspecific activation
by contact with certain
complement proteins
and pathogen.
• No antibody involved
• Called alternate pathway
Fig 16.3 Alternate pathway of complement activation
III. Phagocytosis
• G. Antimicrobial Substances
– 1. Complement System
• c. When
macrophages digest
microbes, they
release a chemical to
stimulate liver to
make proteins
(lectins) that binds to
pathogen and
triggers activation of
complement.
• Called ‘lectin
pathway’
III. Phagocytosis
• G. Antimicrobial Substances
– 2. Interferons (INF) – Antiviral proteins produced in
response to viral infection. Host specific but not virus
specific.
• a. Three types: α, β, and γ interferon
• b. Interferon (α and β) works by inducing uninfected
cells to produce antiviral proteins (AVPs) that prevent
viral replication in surrounding uninfected cells.
• c. γ interferon produced by lymphocytes causes
neutrophils to kill bacteria
• d. They are host-cell-specific, but not virus-specific.
– Now human recombinant INFs produced by genetic
engineering in bacteria. Used to treat viral infections (α for
herpes, hepatitis A and B), β to slow MS
Antiviral action of alpha- and beta- interferons
Figure 16.15 - Overview